Antisepsis in the Time of Antibiotics: Following in the Footsteps of John Snow and Joseph Lister

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If John Snow, a founding father of both anesthesiology and epidemiology, were alive today, undoubtedly he would attack the problem of health care–associated infections (HCAIs) as doggedly as he approached the 1854 cholera epidemic in London.1 Although Snow did not know that Vibrio cholerae was the causative organism, he clearly demonstrated that cholera was communicated by drinking contaminated water from the Broad Street pump. Conversely, in the case of HCAIs associated with surgery, the causative organisms are readily determined, yet the source and mechanism of transmission are frequently unclear. Following in the footsteps of Snow are Koff, Loftus, and their Dartmouth colleagues. They are exploring whether anesthesia providers are the source, or vectors for the transmission, of bacteria that cause surgical site infections (SSIs). In earlier publications, they documented transmission of pathogenic bacteria to the anesthesia operating room work area and established an association between contamination of this area and contamination of IV stopcocks, between contaminated stopcocks and nosocomial infections, and between contamination, nosocomial infection, and hand hygiene by anesthesia providers.2,3
If Joseph Lister, founding father of antiseptic surgery, were alive today, he would be pleased with the low SSI rate today compared with 1867.4 Undoubtedly he would have applied his antiseptic protocols, including carbolic acid, not only to the surgical field and instruments but also to the anesthesia work area and equipment if they had existed in his day. However, in his era, there were no laryngoscopes, bronchoscopes, or endotracheal tubes to pass through bacteria-rich oral and nasal cavities, no spinal or epidural needles or central venous catheters to disrupt the integument, and no anesthesia machines to contaminate. Following in the footsteps of Lister, the Dartmouth group demonstrated that improved hand hygiene by anesthesia providers reduced HCAIs at their institution in their study patients.3 In this issue of Anesthesia & Analgesia, this group goes on to document anesthesia work area and IV stopcock contamination by anesthesia providers in and between operating rooms and between the first and second case in the same operating room, despite application of hand hygiene and anesthesia work area antisepsis protocols typical in modern operating rooms.5
Most anesthesiologists and their quality of care arbiters currently believe that the major contribution of the anesthesia team to the reduction of HCAIs relates to antimicrobial prophylaxis. Unfortunately, approximately 5% of surgical patients continue to experience SSIs despite timely administration of the appropriate antibiotic. In one recent study, intensifying the already rigorous intraoperative antisepsis protocol for surgeons did not reduce SSIs.6 In another, surgical glove perforation did not increase SSIs in patients who received antibiotics.7 If we have reached a plateau in our attempts to lower the SSI rate because we have gone as far as we reasonably can with surgical antisepsis and antimicrobial prophylaxis, then the remaining targets are the patient and the anesthesia provider. Does the work of Koff, Loftus, and others suggest that anesthesia providers have become the typhoid Marys and Johns of the 21st century?8,9 We think these monikers are premature until 4 issues are addressed and resolved: contamination as a surrogate marker versus cause of infection, reproducibility of data, completeness of the data, and consequences of proposed changes in protocols.
Contamination of surgical gloves, instruments, and anesthesia equipment has been demonstrated many times as a function of time from the last cleansing or opening to air and exposure to activity by health care personnel or patients.10–12 However, contamination is not equivalent to infection.
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